|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
HIF-1α-derived cell-penetrating peptides inhibit ERK-dependent activation of HIF-1 and trigger apoptosis of cancer cells under hypoxia.
|
30535970 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Dual-Targeting AKT2 and ERK in cancer stem-like cells in neuroblastoma.
|
31608140 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The expression of p-ERK and Mps1 in CRC with BRAF<sup>V600E</sup> was significantly higher compared with in CRC with BRAF<sup>WT</sup> (P<0.05), and their expression is associated with cancer classification, degree of differentiation and lymph node transfusion (P<0.05).
|
30854056 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Major contributions to reducing prostate cancer cell numbers included low E<sub>2</sub> concentrations producing sustained ERK phospho-activation correlated with generation of reactive oxygen species causing cancer cell death, and phospho-activation of cyclin D1 triggering its rapid degradation by interrupting cell cycle progression.
|
30012504 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Additionally, GLDCV1 increased lactate production and cancer stem cell marker expression and activated ERK and P38 pathways.
|
31773974 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The data show that ERK activation contributes to the overexpression of TIMELESS in cancer.
|
30629587 |
2019 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
After performing single-cell RNA-seq on prostate cancer cell lines and circulating tumor cells from patients, we identified that upregulated gene expression in the EphB2 and Src pathways are associated with advanced malignancy.
|
31805710 |
2019 |
|
Malignant Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
Flow cytometry and western blot analysis demonstrated the fact that anticancer activity was closely related with cancer cell apoptosis and the blockade of the phosphorylation of c-Met and its downstream signaling ERK and Akt.
|
30503936 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
ERK is a newly-identified cancer target molecule, which can significantly control COX-2 in colon cancer cells treated with TGF-β1.
|
31127990 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this review, we summarize our current understanding of the roles of the ERK and JNK pathways in controlling the Warburg effect in cancer and discuss their implication in controlling this metabolic reprogramming in physiological processes and opportunities for targeting their downstream effectors for therapeutic purposes.
|
30487597 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Intestinal mucosal tissue and polyps isolated from Mlkl<sup>-/-</sup> mice exhibited increased ERK activation and elevated expression of genes associated with inflammation and cancer.
|
31158430 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The findings of the present study indicated that Sirt7 affects the malignancy of glioma cells mainly in promoting glioma proliferation and invasion through ERK and STAT3 signaling.
|
30675198 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, the molecular extension of a small fragment bounded at the ERK kinase domain is a valid tactic for the rational synthesis of the ERK inhibitors to control various human malignancies.
|
31717402 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
ERK may play a key role in α2δ1-mediated chemoresistance. mAb 1B50-1 may serve as a potential anti-SCLC drug.<i>Clin Cancer Res; 24(9); 2148-58.©2018 AACR</i>.
|
29437792 |
2018 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Cell-based assays revealed that ibrutinib treatment inhibited cell growth and decreased phosphorylation of ERBB4 and downstream targets MEK and ERK in cancer cell lines with high levels of endogenous ERBB4.
|
29398709 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The RAS/RAF/MEK/ERK pathway is one of the most frequently dysregulated kinase cascades in human cancer, that facilitate the proliferation and survival of cancers driven by growth factor receptors.
|
29393362 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We show that in addition to MEK inhibitors, ERBB receptor and PI3K/mTOR pathway inhibitors are effective in overcoming ERK-inhibitor resistance.<b>Conclusions:</b> These findings suggest that combination therapy with MEK or ERBB receptor or PI3K/mTOR and ERK inhibitors may be an effective strategy for managing the emergence of resistance in the clinic.<i>Clin Cancer Res; 24(16); 4044-55.©2018 AACR</i>.
|
29760222 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In summary, we discovered a novel mechanism of reactivation of the EBV lytic cycle through intracellular iron chelation and induction of ERK-autophagy axis in EBV-positive epithelial malignancies, raising the question whether clinically available iron chelators can be incorporated into existing therapeutic regimens to treat these cancers.
|
30544928 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Proteins encoded by the detected mutated genes activate the two major signaling pathways, also involved in cancer: the RAS/MAPK/ERK pathway and/or the PI3K/AKT/mTOR pathway.
|
29217067 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Consistently, inhibition of SHP2 (also known as PTPN11), which links receptor tyrosine kinase signaling to the RAS-RAF-MEK-ERK pathway<sup>11,12</sup>, was shown to be ineffective in KRAS-mutant or BRAF-mutant cancer cell lines<sup>13</sup>.
|
29808006 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Analysis of metastasis using a tumor xenograft mouse model further confirmed the role of Shc3 <i>in vivo</i> Taken together, our results indicate the importance of Shc3 in HCC progression and identify Shc3 as a novel biomarker and potential therapeutic target in HCC.<b>Significance:</b> Ectopic expression of Shc3 forms a complex with MVP/MEK/ERK to potentiate ERK activation and plays an important role in sorafinib resistance in HCC.<i>Cancer Res; 78(9); 2219-32.©2018 AACR</i>.
|
29330146 |
2018 |
|
Malignant Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
A known major activator of ERK phosphorylation in cancer is oncogenic NRAS and we show that knockdown of NRAS in cells, which bear a Q61 NRAS mutation, sensitises to ER-stress.
|
29329780 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, ephrinB1 depletion by siRNA suppresses EphB2-Fc-induced RhoA activation, and reduces motility and invasiveness of the SW480 and Hs578T human cancer cell lines.
|
29059157 |
2018 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These surprising results delineate a mechanism by which a transcription factor switches cells from ERK to p38 signaling in response to chemotherapy and suggest that therapeutic targeting of HIF1 or the p38 pathway in combination with chemotherapy will block BCSC enrichment and improve outcome in TNBC.<b>Significance:</b> These findings provide a molecular mechanism that may account for the increased relapse rate of women with TNBC who are treated with cytotoxic chemotherapy and suggest that combining chemotherapy with an inhibitor of HIF1 or p38 activity may increase patient survival.<i>Cancer Res; 78(15); 4191-202.©2018 AACR</i>.
|
29880481 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
FGF18 mediated the proliferation of MDA‑MB‑231 cells via the ERK/c‑Myc signaling pathway and induced epithelial‑to‑mesenchymal transition (EMT) factors to promote cancer migration and invasion.
|
29901199 |
2018 |